Journal of Consulting and Clinical Psychology Copyright 2000 by the American Psychological Association, Inc.

2000, Vol. 68, No. 5, 830-842 0022-006X/00/$5.00 DOI: 10.1037//0022-006X.68.5.830

Assessing Symptoms of Attention Deficit Hyperactivity Disorder in

Children and Adults: Which Is More Valid?

Stephen V. Faraone Joseph Biederman

Massachusetts General Hospital, Harvard Medical School, Massachusetts General Hospital
Massachusetts Mental Health Center, and Harvard Institute and Harvard Medical School
of Psychiatric Epidemiology and Genetics

Jennifer A. Feighner Michael C. Monuteaux

Massachusetts General Hospital Massachusetts General Hospital
and Harvard School of Public Health

The assessment of attention deficit hyperactivity disorder (ADHD) in adults has been a source of
controversy. The authors tested competing ideas by evaluating familial transmission among adult and
nonadult relatives of ADHD children. They analyzed ADHD symptom data collected by structured
interviews from the members of 280 ADHD and 242 non-ADHD families. For both past and current
symptoms, both the boys' and girls' families showed significantly more familial aggregation for adult
relatives than for nonadult relatives. The results were similar for inattentive and hyperactive-impulsive
symptoms and for relatives with and without psychiatric comorbidity. The results provide further
evidence for the validity of adult ADHD and support the intriguing idea that, from a familial perspective,
the assessment of ADHD may be more valid in adults than in children. They do not support the idea that
parents of ADHD children are biased to report ADHD symptoms in themselves because of their exposure
to an ADHD child.

Despite media attention and the success of popular books,
investigators continue to debate the validity of attention deficit
hyperactivity disorder (ADHD) in adults. Some assert that most
cases of ADHD remit in adulthood; they conclude that adult
ADHD is very rare (Hill & Schoener, 1996; Shaffer, 1994). If so,
most referred cases must be due to referral artifacts or missed
differential diagnoses. In contrast, others claim that many cases of
ADHD persist into adulthood and that ADHD in adults should be
considered a valid disorder (Barkley, 1997; Murphy & Barkley,
1996a; Spencer, Biederman, Wilens, & Faraone, 1994).
Given this skepticism about the validity of adult ADHD, re-
searchers have sought to assess the validity of the disorder using
the criteria of Robins and Guze (1970). In their view, the validity
of any psychiatric disorder derives not from a single study, but
Stephen V. Faraone, Pediatric Psychopharmacology Unit, Child Psychi-
atry Service, Massachusetts General Hospital (MGH); Harvard Medical
School; Massachusetts Mental Health Center; and Harvard Institute of
Psychiatric Epidemiology and Genetics. Joseph Biederman, Pediatric Psy-
chopharmacology Unit, Child Psychiatry Service, MGH; and Harvard
Medical School. Jennifer A. Feighner, Pediatric Psychopharmacology
Unit, Child Psychiatry Service, MGH. Michael C. Monuteaux, Pediatric
Psychopharmacology Unit, Child Psychiatry Service, MGH; and Depart-
ment of Epidemiology, Harvard School of Public Health.
This work was supported in part by National Institutes of Health Grants
R01MH57934, R01HD37694, R13MH59126, and R01MH41314.
Correspondence concerning this article should be addressed to Stephen
V. Faraone, Pediatric Psychopharmacology Unit (ACC 725), Massachu-
setts General Hospital, 15 Parkman Street, Boston, Massachusetts 02114.
Electronic mail may be sent to sfaraone@earthlink.net.
from a pattem of consistent data. For psychiatric disorders, stan-
dard validation criteria include clinical correlates, treatment re-
sponse, laboratory studies, follow-up studies, and family history.
Our prior reviews of these validity criteria suggest ADHD may be
a valid disorder (Faraone, 2000; Spencer et al., 1994; Spencer,
Biederman, Wilens, & Faraone, 1998).
If adult ADHD is valid, we would expect the children of ADHD
adults to have an elevated prevalence of ADHD (Faraone, Tsuang,
& Tsuang, 1999; Faraone & Tsuang, 1995). This has been found
by the two extant family studies of adult ADHD (Biederman, et al.,
1995; Manshadi, Lippmann, O'Daniel, & Blackman, 1983). These
studies both produced the same intriguing result: The risk of
ADHD among children of ADHD adults was much higher than the
risk for ADHD among relatives of children with ADHD. For
example, we found a 57% prevalence of ADHD among children of
ADHD adults, which was much higher than the 15% prevalence of
ADHD among siblings of ADHD children (Biederman et al.,
1995). These results are somewhat counterintuitive. If adult
ADHD is an uncertain diagnosis, fraught with the difficulties of
retrospective recall and self-referral biases, there should be more
false positive cases of ADHD among adults than among children.
If that were the case, then evidence for familial transmission
should be lower in families sampled through adults compared with
those sampled through children. Yet the opposite is true.
The high familial loading of adult ADHD suggests that genes
(or other familial risk factors) may play a smaller role in the
etiology of remitting ADHD than they do for persistent ADHD.
We tested this persistence hypothesis in two ways. In a prospective
study, we examined 140 ADHD boys and 120 non-ADHD boys at
a baseline assessment and completed a 4-year follow-up study. By

830
 VALIDITY OF ASSESSINGADULT ADHD SYMPTOMS
mid-adolescence, 85% of the ADHD boys continued to have the
disorder; 15% remitted. The prevalence of ADHD was signifi-
candy higher among the relatives of persistent ADHD probands
compared with relatives of remitted ADHD probands (Biederman,
et al., 1996). Parents of persistent ADHD probands were 20 times
more likely to have ADHD than parents of controls whereas
parents of nonpersistent ADHD probands showed only a fivefold
increased risk. Similarly, siblings of persistent ADHD probands
were 17 times more likely to have ADHD than siblings of controls,
whereas siblings of nonpersistent ADHD probands showed only a
four-fold increased risk (Faraone, Biederman, & Monuteaux,
2000). In a retrospective study, we compared ADHD adolescents
having retrospectively reported childhood onset ADHD with
ADHD children. The relatives of adolescent probands had higher
rates of ADHD compared with the relatives of child probands
(Biederman et al., 1998). Thus, a prospective study of children and
a retrospective study of adolescents suggest that, when ADHD
persists into adolescence and adulthood, it is highly familial.
Taken together, these data suggest that, from a familial perspec-
five, not only is the adult ADHD diagnosis valid, but it might
actually be more valid than the childhood diagnosis. By more valid
we mean that a validity coefficient indexing the familial transmis-
sion of ADHD would be greater for adults than children. This idea
makes a straightforward prediction: When selecting families
through ADHD children, the evidence for familial transmission
should be greater when examining the risk to adult relatives than
it is when examining the risk to non-adult relatives. Although this
prediction is straightforward, testing it is complicated by uncer-
tainties about the correct symptoms threshold for defining ADHD
in adults.
Although extensive psychometric studies provided empirical
support for the symptom thresholds used to diagnose ADHD in
children (Lahey et al., 1994), little is known about the validity of
these symptom thresholds for adult ADHD. Barkley (1998) sug-
gested that applying current ADHD criteria to adults is not devel-
opmentally sensitive. The fourth edition of the Diagnostic and
Statistical Manual of Mental Disorders (DSM-IV; American Psy-
chiatric Association, 1994) recognizes developmental changes in
the expression of ADHD in several ways. It cautions diagnosti-
cians that, with maturation, symptoms become less conspicuous.
Older children may be restless and fidgety but not overly hyper-
active. With age, inattention may predominate as school tasks
require increasing levels of attention. The DSM also specifies that
symptoms are considered present only if they are maladaptive and
inconsistent with developmental level. The DSM-IV also includes
the category of ADHD in partial remission for individuals (espe-
cially adolescents and adults) who currently have symptoms but no
longer meet full criteria.
The net effect of developmental changes is to make it more
difficult for ADHD children to meet criteria for the disorder as
they get older. This situation was shown empirically by Murphy
and Barkley (1996b), who used self-report rating scales to diag-
nose ADHD in 720 adults applying for or renewing their drivers
licenses in the state of Massachusetts. In this population sample of
adults, they found a systematic decrease in the prevalence of
ADHD symptoms with age. Although this decrease may indicate
true remission of symptoms with age, it may also indicate a
measurement problem: reduced sensitivity of ADHD symptoms
with age. If the latter is true, then using the same symptom
831
threshold to define deviance at each age will reduce the number of
diagnosable cases among older individuals.
This issue was addressed by Heiligenstein, Conyers, Berns,
Miller, and Smith (1998). They examined ADHD diagnoses and
symptom scores among 448 college students not selected for any
psychiatric diagnosis. Four percent of the students met DSM-IV
criteria for ADHD. They then defined ADHD as deviance from the
norm: Students were defined as having ADHD if their total symp-
tom score exceeded the 93rd percentile of the sample. The subjects
who met this criterion showed clinically significant symptoms
(Heiligenstein, Guenther, Levy, Savino, & Fulwiler, 1999; Heiligen-
stein & Keeling, 1995). Thus, the authors argued that the DSM-IV
criteria were too stringent because they did not identify many
subjects who were both deviant from the norm and showed symp-
toms warranting clinical attention.
The choice of a symptom threshold also affects estimates of the
persistence of ADHD into adulthood. For example, Fischer (1997)
followed 148 hyperactive children for 15 years. At a mean age
of 21, the self-report of these participants indicated that only 3%
met criteria for ADHD as defined by the revised 3rd edition of the
DSM (DSM-III-R; American Psychiatric Association, 1987). But
when they used a psychometric criterion to define ADHD (symp-
toms exceeding the 93rd percentile of severity of the control
group), 25% met criteria for ADHD. We reported similar findings
from our longitudinal study of ADHD boys (Biederman, Mick, &
Faraone, 2000). We found that by the age of 19, 38% of children
had the full ADHD diagnosis, 72% showed persistence of at least
one-third of the symptoms required for the diagnosis, and 90%
showed evidence of clinically significant impairment.
These considerations have led to the idea that ADHD be recast
as a norm-referenced rather than a criterion-referenced diagnosis
(Barkley, 1998; Faraone, 2000). This idea suggests that one deal
with the diagnosis of ADHD as one does the constructs of adaptive
functioning or intelligence. For example, one would not have
adults complete the Wechsler Intelligence Scales for Children and
then conclude that intelligence increases with age. Instead, one
uses different test batteries for different age groups; within a single
battery, a score is considered high or low in reference to people of
the same age.
These uncertainties about the developmental course of ADHD
symptoms raise a key question about the decline of ADHD symp-
toms over time: Does this decline reflect remission of the disorder,
decreases in severity with age, or both? Or is this decline an
artifact of measurement because the symptoms used to define
ADHD in children are not sensitive1 measures of ADHD in adult-
hood? Although the answers to these questions must await future
research, the issues they raise suggest that studies of adult ADHD
examine the disorder in a manner that attends to the potential
reduced sensitivity of the diagnosis in adulthood.
In summary, family studies suggest not only that the adult
ADHD diagnosis is valid, but also that it might actually be more
valid than the childhood diagnosis (i.e., ADHD that persists into
adulthood is more familial than ADHD that remits in childhood).
Our prior work has shown (a) children of clinically referred
ADHD adults have very high rates of ADHD (Biederman et al.,
l In this context, sensitivity is the probability that the diagnosis of
ADHD will correctly identify an ADHD adult as having ADHD.
832 FARAONE, BIEDERMAN, FEIGHNER, AND MONUTEAUX
1995), and (b) in both retrospective (Biederman et al., 1998) and
prospective (Biederman, Faraone, Milberger, et al., 1996; Faraone,
2000) studies, w h e n A D H D persists into adolescence and young
adulthood, it is highly familial.
Our prior studies have addressed the implications of persistence
by looking at the relatives o f persistent and nonpersistent A D H D
probands. They have not, however, examined persistence in the
relatives. If our hypothesis about persistence is correct, then evi-
dence for familial transmission should be greater w h e n examining
the risk to adult relatives (parents and adult siblings) than it is
w h e n examining the risk to nonadult relatives (other siblings).
Thus, this report sought to extend our prior work by testing this
prediction. Moreover, given the uncertainties about h o w to diag-
nose A D H D in adults, the present article sought to address this
issue in a manner that would deal with the effects o f varying
s y m p t o m thresholds. W e did so by using receiver operating char-
acteristic (ROC) analyses o f A D H D symptoms among relatives
ascertained in our two previously reported family studies o f
A D H D (Biederman et al., 1999; Biederman et al., 1992).
Method
Participants
We analyzed data from two family-genetic studies of ADHD that we
have presented in previous publications (Biederman et al., 1999, 1992).
Our family study of ADHD boys selected two groups of index male
participants: 140 ADHD probands and 120 boys without ADHD compar-
isons. These groups had 454 and 368 first-degree biological relatives,
respectively. Our family study of ADHD girls studied two groups of index
female participants: 140 ADHD probands and 122 girls who did not have
ADHD. These groups had 417 and 369 first-degree biological relatives,
respectively, who provided data.
All probands were between the ages of 6 and 17. Potential probands
were excluded if they had been adopted or if their nuclear family was not
available for study. We excluded children if they had major sensorimotor
handicaps (e.g., paralysis, deafness, blindness), psychosis, autism, or an
estimated Full-Scale IQ score less than 80. Also, to minimize the potential
confounds of extreme social adversity, we excluded participants from the
lowest Hollingshead-Redlich socioeconomic class. Each of the ADHD
probands met diagnostic criteria for current ADHD at the time of the
clinical referral; at the time of recruitment, each had active symptoms of
the disorder.
Two independent sources provided the proband children. We selected
psychiatrically referred ADHD probands from consecutive referrals to the
Pediatric Psychopharmacology Unit at the Massachusetts General Hospital
(MGH). At MGH, we recruited normal controls from the Pediatric Ambu-
latory Service. The Harvard Community Health Plan provided both pedi-
atrically referred ADHD and control probands. We screened controls only
for the presence of ADHD.
Procedure
Psychiatric assessments of participants and siblings relied on the Sched-
ule for Affective Disorders and Schizophrenia for School-Age Children:
Epidemiologic Version (Kiddie SADS-E; Orvaschel & Puig-Antich, 1987).
For the probands nonadult siblings, and adult siblings, we collected
maternal- and self-reports of symptoms, except for children younger
than 12 years of age, who were not directly interviewed. The assessment
personnel were blind to participant diagnosis and ascertainment site. For
parents, we collected self-reports of symptoms using the Structured Clin-
ical Interview for DSM-III-R (SCID; Spitzer, Williams, Gibbon, & First,
1990), supplemented with modules from the Kiddie SADS-E covering
childhood diagnoses. We collected data on nearly all the parents: 99% for
control boys, 100% for boys with ADHD, 98% for control girls, and 98%
for girls with ADHD. Assessments of parents were masked with regard to
proband diagnosis. All parents signed a written consent form prior to
participation in the study.
To be given a diagnosis of adult ADHD, the participant must have met
the following criteria: (a) On the basis of their retrospective report, par-
ticipants must have met DSM-III-R criteria for a diagnosis of ADHD by
the age of 7; (b) they must have had at least five DSM-III-R symptoms of
ADHD at the time of assessment; and (c) they must have described a
chronic course of ADHD symptoms from childhood to adulthood. To elicit
ADHD symptoms, we used the ADHD module from the Kiddie- SADS-E,
wording questions in the past tense. Thus, the symptoms used to assess
childhood ADHD and current adult ADHD were identical. We assessed
chronicity of symptoms by inquiring about the presence of symptoms
during childhood, adolescence, and adulthood.
The five interviewers had undergraduate degrees in psychology; they
were trained to high levels of interrater reliability. The principal investi-
gator, Joseph Biederman supervised the interviewers throughout the study.
We computed kappa coefficients of agreement by having three experi-
enced, board-certified child and adult psychiatrists diagnose participants
from audio-taped interviews made by the assessment staff. On the basis
of 61 interviews, all disorders achieved kappas higher than 0.82, with the
exception of alcohol abuse, which was 0.75. The mean kappa was 0.90.
Kappas of 1.0 were obtained for ADHD (95% confidence interval: 0.8-
1.0), substance abuse (0.7-1.0), and substance dependence (0.7-1.0). Al-
though these kappa coefficients showed high interrater agreement, they did
not demonstrate the validity of the diagnoses. Full information regarding
kappa coefficients is available on request.
A committee of four board-certified child and adult psychiatrists re-
solved all diagnostic uncertainties. The committee members were blind to
the participants' ascertainment group, ascertainment site, and all data
collected from other family members. For children older than 12 years, the
diagnosticians combined data from interviews of children with data from
interviews of mothers about their children by considering a diagnostic
criterion positive if endorsed in either interview.
Statistical Analysis
Our analyses sought to test one main hypothesis: When selecting fam-
ilies through ADHD children, the evidence for familial transmission should
be greater for the risk to adult relatives than for the risk to nonadult
relatives. We used a combination of logistic regression and ROC analysis
to provide a full examination of how varying symptom thresholds might
affect evidence for familial transmission. Before testing our study hypoth-
esis, we examined demographic and clinical features of the sample and
determined if these were associated with either ADHD or age of relative.
These analyses used logistic regression (for binary outcomes) or linear
regression (for continuous outcomes).
To test our hypothesis, we estimated several sets of logistic regression
models separately for boy and girl proband families. Each model used
proband status (ADHD and controls) as the dependent variable and number
of ADHD symptoms in relatives as the independent variable. We let p
denote the probability that the relative comes from an ADHD family (i.e.,
a family ascertained through a participant with ADHD). Then, log[p/(1 -
p)] is the logit ofp. Logistic regression models the logit as a linear function
of the number of ADHD symptoms in the adult and nonadult relatives. For
each model, the magnitude and significance of familial transmission was
assessed by the estimated coefficient for the symptom variable as a pre-
dictor of group status. This regression coefficient (/30 indicates the change
in the logit associated with an increase of one in the relative's ADHD
symptom count. Exp(/3i) is the odds ratio, that is, the ratio of the odds that
a relative with N symptoms comes from an ADHD family compared with
a relative who has N - 1 symptoms. Thus, the odds ratio is an index of the
 VALIDITY OF ASSESSING ADULT ADHD SYMPTOMS
degree of familial transmission. An odds ratio of 1.0 signifies no familial
transmission. As the odds ratio increases above 1.0, so does evidence for
the familial transmission of ADHD. We assessed the significance of/3 i
(and hence of the odds ratio) by a z score ([Ji/SE[~]).
We tested two logistic regression models for current ADHD symptoms.
Model 1 was as follows: number of current ADHD symptoms for adult
relatives (age greater than 18) as a predictor of proband diagnosis. Model 2
was as follows: number of current ADHD symptoms for nonadult relatives
as a predictor of proband diagnosis. Our hypothesis predicted that the odds
ratios that index familial transmission should be greater for Model 1
compared with Model 2. We tested this hypothesis using a likelihood ratio
chi-square test. We also tested a parallel set of models for the relative's past
history of ADHD symptoms. Then, to explore the effects of ascertainment
site and psychiatric comorbidity, we repeated these analyses after stratify-
ing the participants on these variables. We also separately examined past
and current symptoms for the two main clusters of ADHD symptoms:
hyperactive-impulsive and inattentive.
For analyses of current symptoms, we excluded child or adult relatives
who were being treated for ADHD at the time of assessment. The numbers
(and percentages of total relatives) excluded were as follows: 33 child
relatives of girl probands (15%), 16 adult relatives of girl probands
(3%), 10 child relatives of boy probands (4%), and 5 adult relatives of boy
probands (1%).
Because relatives from the same family are not statistically independent
from one another, standard logistic regression methods will produce inac-
curate p values. To address this intrafamily clustering, we adjusted vari-
ance estimates using Huber's (1967) formula as implemented in STATA
(Stata Corporation, 1997). This formula is a theoretical bootstrap that
produces robust statistical tests. The method works by entering the cluster
scores (i,e., sum of scores within families) into the formula for the estimate
of variance. The resulting p values are valid even when observations are
not statistically independent of one another.
We used the logistic regression models to generate ROC curves as
follows. Each model allows us to compute two statistics that assess the
degree to which each possible number of ADHD symptoms in relatives
discriminates the relatives of ADHD probands from the relatives of control
probands. These statistics are sensitivity and the false positive rate. In this
context, sensitivity refers to the proportion of ADHD probands that have a
relative with N or more symptoms. Thefalse positive rate is the proportion
of control probands that have a relative with N or more symptoms. We can
then compute a pair of sensitivity and false positive rate statistics for each
number of ADHD symptoms. To plot the ROC curve, all possible pairs of
sensitivity and false positive rate values are joined into one curve by
plotting sensitivity on the vertical axis and the false positive rate on the
horizontal axis (McNeil & Hanley, 1984).
If ADHD symptoms are familial, then the ROC curve should rise above
the diagonal line connecting the [0, 0] and [1, 1] points of the ROC graph.
If, as our hypothesis predicts, symptoms in adult relatives are more familial
than symptoms in child relatives, then the ROC curve for adults should rise
above the curve for children. That is, the area under the adult relative's
curve should be greater than the area under the child relative's curve. We
tested this difference using the method of Hanley and McNeil (1983).
Results
Clinical and Demographic Data
Table 1 presents the clinical and demographic features of the
adult and child relatives of ADHD boys. It shows that, compared
with control probands the relatives of ADHD probands came from
lower social classes and less intact families. Adult relatives did not
differ from child relatives on these demographic features. Table 1
also shows that the relatives of ADHD probands were at higher
risk for ADHD, conduct disorder, major depression, and anxiety
833
disorders. Major depression and anxiety disorders were more prev-
alent in the adult sample, and ADHD was more prevalent in the
child sample. This latter effect was seen for both the hyperactive-
impulsive and inattentive total symptom counts, whether measured
currently or in the past.
Table 2 presents the same information for relatives of ADHD
girls. Relatives of ADHD probands were slightly younger than
relatives of controls, and the adult relatives came from a somewhat
lower social class than the child relatives. Relatives of ADHD girl
probands were at higher risk for ADHD, major depression, and
anxiety disorders but not conduct disorder. ADHD was more
prevalent in the child compared with the adult sample of relatives.
These lower rates of ADHD were seen for both the hyperactive-
impulsive and inattentive total symptom counts whether measured
currently or in the past.
Analyses of Current Symptoms
Table 3 provides a summary of the logistic regression analyses.
For the analyses of current symptoms, the results were identical for
the relatives of boy and girl probands. Both showed statistically
significant familial aggregation for adult relatives but not for
nonadult relatives. Moreover, for both samples, the differences
between the adult and nonadult samples were statistically signifi-
cant: boys, X~(1, N = 776) = 10.9, p = .001; girls, X~(1, N =
735) = 11.6, p < .001. The pattern of results can be seen in the
odds ratios. These ratios indicate the increased odds of being a
relative of an ADHD proband afforded by an increment of one in
the level of the relative's ADHD symptoms count.
The implications of the logistic regression analyses can be seen
in Figure 1. Panel A shows ROC curves separately for adult and
nonadult relatives of boy probands. If ADHD were not familial,
the points on the ROC curve would fall on the diagonal line
connecting the [0, 0] and [1, 1] points. Points lying above the
diagonal provide evidence for familial transmission.
Each point on the graph indicates, for a different diagnostic
threshold, N, the proportion of ADHD probands that have a rela-
tive with N or more symptoms (the vertical axis) and the propor-
tion of non-ADHD probands that have a relative with N or more
symptoms (the horizontal axis). For example, the point labeled
"A" in Panel A of Figure 1 shows that 30% of ADHD probands
have an adult relative with two or more current symptoms. In
contrast, only 10% of control probands have an adult relative with
two or more current symptoms. If we move down the ROC curve
toward the [0, 0] point, the next point we encounter tells us that
21% of ADHD probands, but only 6% of controls, have an adult
relative with three or more current symptoms. The point labeled
"B" shows that 30% of ADHD and 25% of control probands have
a nonadult relative with two or more current symptoms. Moving
down the ROC curve toward the [0, 0] point, the next point we
encounter tells us that 23% of ADHD probands and 19% of
controls have a nonadult relative with three or more current
symptoms.
Consistent with the logistic regression analyses, the area under
the adult ROC curve is greater than the area under the nonadult
curve, indicating that ADHD is more familial in the adult com-
pared with the nonadult relatives (z = 3.0, p = .001). The data
from the sample of families selected through girl probands show
834 FARAONE, BIEDERMAN, FEIGHNER, AND MONUTEAUX

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836 FARAONE, BIEDERMAN, FEIGHNER, AND MONUTEAUX

Table 3
Results of Logistic Regression Models by Gender of Proband
Description of model Statistical results

Sample Source of symptoms Type of relative Odds ratio z p

Boys Current Adult 1.4 5.2 <.001

Current Nonadult 1.1 1.6 .12
Past Adult 1.3 6.3 <.001
Past Nonadult 1.1 2.9 .003
Girls Current Adult 1.3 6.0 <.001
Current Nonadult 1.0 0.4 .68
Past Adult 1.3 7.7 <.001
Past Nonadult 1.1 2.7 .008

the same pattern of results (see Panel B of Figure 1; z = 3.4, p <
.001).
Analyses of Past Symptoms
For the analyses of past symptoms, Table 3 shows that the
results for the boys and girls samples were very similar. Both
showed statistically significant familial aggregation for both adult
and nonadult relatives. Notable was that the odds ratios show that
the direction of effect was similar for boys and girls. Both showed
greater odds ratios for adult compared with nonadult relatives.
These differences between the adult and nonadult samples were
statistically significant: boys, X~(1, N = 791) = 5.3, p = .021;
girls, X~l(1, N = 784) = l l . 4 , p < .001.
Figure 2 shows the ROC curves for past symptoms. As we saw
for current symptoms, the results from the boys and girls samples
are similar. The areas under both adult ROC curves are greater
than the areas under the corresponding nonadult curves, indicating
that ADHD is more familial in the adult compared with the
nonadult relatives (boys: z = 2.2, p = .014; girls: z = 3.1, p <
.001).
Analyses of Ascertainment Source, Symptom Clusters, and
Psychiatric Comorbidity
Table 4 shows that the results were very similar when we
stratified the samples by ascertainment source using analyses that
combined relatives of boy and girl probands. With the exception of
current symptoms for nonadult relatives, both clusters of symp-
toms showed statistically significant familial aggregation for both
adult and nonadult relatives. The odds ratios show that the direc-
tion of effect was similar for both ascertainment sites. Both show
greater odds ratios for adult compared with nonadult relatives.
These differences between the adult and nonadult samples were
statistically significant: M G H current symptoms, X~(1, N =
653) = 24.4, p < .001; M G H past symptoms, X~(1, N =
700) = 14.1, p < .001; health maintenance organization (HMO)
current symptoms, X~I(1, N = 858) = 6.2, p = .013; HMO past
symptoms, X~I(1, N = 875) = 10.1, p = .002.
Table 5 shows that the results were very similar when inatten-
tive and hyperactive-impulsive symptoms were considered sepa-
rately. The Appendix shows how these clusters were defined with
DSM-III-R symptoms. These analyses combine relatives of boy
and girl probands. With the exception of current symptoms for
nonadult relatives, both clusters of symptoms showed statistically
significant familial aggregation for both adult and nonadult rela-
tives. The odds ratios show that, for both types of symptoms, the
odds ratios were greater for adult compared with nonadult rela-
tives. These differences between the adult and nonadult samples
were statistically significant: current inattentive symptoms, )d~(1,
N = 1,510) = 21.5, p < .001; past inattentive symptoms, X~(1,
N = 1,575) = 18.7, p < .001; current hyperactive-impulsive
symptoms, X~(1, N = 1,511) = 22.9, p < .001; past hyperactive-
impulsive symptoms, X~I(I, N = 1,575) = 18.1, p < .001.
Table 6 shows the results stratified by psychiatric comorbidity.
For the analyses labeled "No Diagnosis," we included only rela-
tives who did not have any of the following disorders: conduct
disorder, major depressive disorder with severe impairment, mul-
tiple anxiety disorder, or antisocial personality disorder. Relatives
with one or more of these diagnoses were included in the analyses
labeled "At Least One Diagnosis." These analyses combined rel-
atives of boy and girl probands. With the exception of current
symptoms for nonadult relatives, both clusters of symptoms
showed statistically significant familial aggregation for both adult
and nonadult relatives. The odds ratios show that the direction of
effect was similar for both the comorbid and non-comorbid groups.
Both show greater odds ratios for adult compared with nonadult
relatives. These differences between the adult and nonadult sam-
ples were statistically significant--no diagnoses, current symp-
toms, X~I(1, N = 1,090) = 13.6, p < .001; no diagnoses, past
symptoms, X~I(1, N = 1,120) = 15.6, p < .001; and one or more
diagnoses, current symptoms, X~l(1, N = 386) = 5.9, p = . 0 1 5 -
with the exception of the case of past symptoms for relatives
having one or more diagnosis, X~(1, N = 418) = 2.5, p = 0.114.
Analyses of Reporter Bias Effects
Because adult relatives of ADHD children may be aware of the
ADHD symptoms in their proband children, they may be biased to
report ADHD symptoms in themselves. If so, our finding of
greater familiality in adult relatives might be due to this reporter
bias effect. This type of reporter bias makes a testable prediction:
The adult relatives of ADHD children should have a greater
number of symptoms than the nonadult relatives. Inspection of
Tables 1 and 2 shows that this prediction does not hold. For both
the boys and girls samples, the mean number of symptoms re-
ported by adult relatives of ADHD probands was nonsignificantly
 VALIDITY OF ASSESSING ADULT ADHD SYMPTOMS 837

IA: Current Symptoms Among Relatives of Boy ADHD and Control Probands
o denotes adult relatives, A denotes child relatives
1-

,9-

,8

.7-

.6-

.5-
.4-
.3-

.2"

.1-

O-
o' '1 .'2 ~3 14 .
'5 '.6 .; .'8 ~9 ;
False Positive Rate
IB: Current Symptoms Among Relatives of Girl ADHD and Control Probands
o denotes adult relatives, A denotes child relatives
1

,9

.8-

.7-

.5-

.4-
r~
.3"

.2-

.I"

0-
i |
~) •I1 .2' .3= .4 .5 •'6 ,'7 .I8 ~9 1
False Positive Rate

Figure 1. Receiver operating characteristic curves for current ADHD symptoms among relatives of boy and
girl ADHD participants. ADHD = attention deficit hyperactivity disorder.

less than the mean number of symptoms reported by nonadult
relatives. This was true for current and past symptoms and for
inattentive and hyperactive-impulsive symptoms (all ps > .05).
Discussion
Our results support the study hypothesis: When selecting fam-
ilies through ADHD children, evidence for familial transmission is
greater when examining ADHD symptoms in adult relatives than
it is when examining symptoms in nonadult relatives. Thus, our
results provide further evidence for the validity of adult ADHD
and continue to support the intriguing idea that, from a familial
perspective, the diagnosis of ADHD is more valid in adults than it
is in children.
The pattern of results supporting this hypothesis was seen for
both current and past assessments of total ADHD symptoms and
for inattentive and hyperactive-impulsive symptoms considered
separately. Moreover, our results cannot be accounted for by
gender, psychiatric comorbidity, or ascertainment source because
we found the same pattern of results for the subgroups defined by
these variables.
We also considered the possibility that ADHD in children biases
the self-reports of ADHD in their adult relatives. The adult rela-
tives of ADHD children are usually aware of the ADHD symptoms
in the child. That knowledge may bias them to report ADHD
symptoms in themselves. If that occurs, then the rates of ADHD
among adult relatives of ADHD children would be spuriously
838 FARAONE, BIEDERMAN, FEIGHNER, AND MONUTEAUX

2A: Past Symptoms Amon~ Relatives of Boy ADHD and Control Probands
o denotes adult relatives, A denotes child relatives
1

.8

.8-

.7

~ .4-
r~
.3-

.2"

.1

0
!
I . .
0 '1 2 '3 ,I 5
I 16
7
= .i9
1'
False Positive Rate
2B: Past Symptoms Among Relatives of Girl ADHD and Control Probands
o denotes adult relatives, A denotes child relatives
1 -

.9-

.8-

.7-

.~ .5-

.4-

.3-

.2 ~

,I-

0-
¢
.
0 . .
.1 . .
.2 . .3 . .4 .5
False Positive Rate
. . '7. . '8 ,, 1,

Figure 2. Receiver operating characteristic curves for past ADHD symptoms among relatives of boy and girl
ADHD participants. ADHD = attention deficit hyperactivity disorder.

high, leading to the incorrect conclusion that adult ADHD is more
familial than child ADHD. But if ADHD adults are biased to
overreport symptoms, then the adult relatives of ADHD children
should have had a greater number of symptoms than the child
relatives. That was not the case. In fact, the adult relatives tended
to report fewer symptoms, although the difference was not statis-
tically significant.
We have made two statements that appear contradictory but are
not: (a) Adult ADHD symptoms are more familial than child
ADHD symptoms, and (b) the number of ADHD symptoms does
not differ between adult and child relatives. The statements do not
contradict one another because any index of familial transmission
must measure differences between two quantities: the number of
ADHD symptoms in ADHD relatives and the number of symp-
toms in control relatives (Faraone et al., 1999). Our finding that
ADHD is more familial among adult relatives is due to symptom
differences between child and adult relatives of controls. Because
the adult relatives of controls had fewer symptoms than the child
relatives of controls, the ADHD versus control comparison is
greater for adult relatives.
This feature of our data can be seen by inspecting the ROC
curves. Recall that each successive point on the ROC shows the
sensitivity and false positive rate for successive ADHD symptom
thresholds. For example, the point labeled "A" in Panel A of
Figure 1 shows that 30% of ADHD probands and 10% of control
probands have an adult relative with two or more current symp-
toms. Compare this point with the point labeled "B," which shows
that 30% of ADHD and 25% of control probands have a nonadult
 VALIDITY OF ASSESSING ADULT ADHD SYMPTOMS 839

Table 4
Results of Logistic Regression Models by Ascertainment Source

Description of model Statistical results

Source Source of symptoms Type of relative Odds ratio z

HMO Current Adult 1.2 5.2 <.001

Current Nonadult 1.1 1.2 .231
Past Adult 1.2 6.7 <.001
Past Nonadult 1.1 1.4 .153
MGH Current Adult 1.4 5.6 <.001
Current Nonadult 1.0 0.3 .735
Past Adult 1.3 6.9 <.001
Past Nonadult 1.1 3.4 .001

Note. HMO = health maintenance organization; MGH = Massachusetts General Hospital.

relative with two or more current symptoms. These points tell us
that, for the identical symptom threshold used to define ADHD
(two or more), the sensitivity for adult relatives is identical to that
for child relatives. In contrast, the false positive rate for child
relatives is more than twofold that of adult relatives.
If we move down the ROC curve toward the [0, 0] point, the
next point we encounter on the adult relative curve tells us that
21% of ADHD probands but only 6% of controls, have an adult
relative with three or more current symptoms. Moving down the
child ROC curve, we see that 23% of ADHD probands and 19% of
controls have a nonadult relative with three or more current symp-
toms. Thus, at the threshold of three or more symptoms, child and
adult relatives have a similar sensitivity. But, as we saw for points
A and B, the child relatives have a greater false positive rate than
the adult relatives.
The false positive rate for each symptom threshold is the pro-
portion of control probands that have a relative whose symptoms
exceed the threshold. Thus, from a familial perspective, we have
shown that the diagnosis of ADHD yields more false positives in
nonadult than adult relatives. This idea is counterintuitive given
contemporary skepticism about the diagnosis of adult ADHD
(Shaffer, 1994). If the self-report of adult ADHD is heavily influ-
enced by recall biases and reports in the media, we should have
found it to be less valid and more prone to false positive reports
than the diagnosis of ADHD among youths.
Although our data cannot rule out the possibility of some biased
reports of ADHD in adults, our evidence against reporter bias is
consistent with our prior report from a different sample. In that
study, we compared symptom rates between 26 clinically referred
ADHD adults who had ADHD children and 49 clinically referred
ADHD adults who did not have ADHD children (Faraone, Bied-
erman, & Mick, 1997). We hypothesized the following: If having
an ADHD child biased an adult to report ADHD symptoms, then
ADHD adults having ADHD children should have reported more
symptoms than ADHD adults who did not have ADHD children.
We rejected that hypothesis by showing that the number of symp-
toms reported by ADHD adults did not differ between those who
did and did not have ADHD children. Moreover, no individual
symptom was more frequent among the ADHD adults who had
ADHD children compared with those who did not have ADHD
children. Thus, having an ADHD child did not bias ADHD adults
to overreport ADHD symptoms.
Our results also address the idea that ADHD should be recast as
a norm-referenced rather than a criterion-referenced diagnosis
(Barkley, 1998; Faraone, 2000). As we reviewed in the introduc-
tion, some have argued that the symptom threshold for diagnosing
adult ADHD should be lower than that for diagnosing ADHD in
youths. The ROC curves addressed this issue because if a symptom
threshold that defines a specific point also defines a familial form
of ADHD, then that point should lie above the diagonal line
connecting the [0, 0] and [1, 1] points. All of the four curves for
adult relatives notably show the same finding: All of the points on
the ROC lie above the diagonal. Thus, from a familial perspective,
any of these points could be used as a symptom threshold to define

Table 5
Results of Logistic Regression Models for ADHD Symptom Clusters

Description of model Statistical results

ADHD symptom cluster Source of symptoms Type of relative Odds ratio z

haattentive Current Adult 1.5 6.9 <.001

Current Nonadult 1.1 1.2 .241
Past Adult 1.4 9.3 <.001
Past Nonadult 1.1 2.9 .003
Hyperactive/Impulsive Current Adult 1.5 6.9 <.001
Current Nonadult 1.1 1.0 .318
Past Adult 1.5 9.2 <.001
Past Nonadult 1.2 3.7 <.001

Note. ADHD = attention deficit hyperactivity disorder.

840 FARAONE, BIEDERMAN, FEIGHNER, AND MONUTEAUX

Table 6
Results of Logistic Regression Models Stratified by Psychiatric Comorbidity

Description of model Statistical results

Diagnostic statusa Source of symptoms Type of relative Odds ratio z p

No diagnoses Current Adult 1.3 5.1 <.001

Current Nonadult 1.0 1.0 .332
Past Adult 1.3 7.2 <.001
Past Nonadult 1.1 2. l .038
At least one diagnosis Current Adult 1.2 4.0 <.001
Current Nonadult 1.0 0.0 .974
Past Adult 1.2 5.2 <.001
Past Nonadult 1.1 2.0 .047

aRefers to the presence of at least one of the following: conduct disorder, major depressive disorder with severe
impairment, multiple anxiety disorder, or antisocial personality disorder.

adult ADHD. We do not suggest that clinical symptom thresholds
be chosen soley on familial data. Studies addressing the clinical
significance of specific thresholds, in the context of appropriate
normative data, are needed.
This finding is in line with the idea that we should view ADHD
as a dimensional trait, not a discrete category. There are several
lines of evidence that suggest strongly that a dimensional perspec-
tive on ADHD is valid. First, many studies have found an excellent
correspondence between dimensional measures of ADHD (e.g.,
scales derived from the Child Behavior Checklist, the Conners
Scales, and the Strengths and Difficulties Questionnaire) and the
categorical diagnosis of ADHD (Biederman et al., 1993; Bieder-
man, Faraone, Mick, Moore, & Lelon, 1996; Bird, et al., 1987;
Boyle et al., 1997; Chen, Faraone, Biederman, & Tsuang, 1994;
Edelbrock, 1986; Hudziak, 1997). These studies suggest that chil-
dren with ADHD are at one extreme of a quantitative dimension,
and that on this quantitative dimension, there is no obvious bimo-
dality that separates ADHD children from non-ADHD children.
Further support for the validity of a quantitative approach to
ADHD is the fact that quantitative measures of ADHD are highly
heritable (about 70%) and as heritable as the ADHD diagnosis
(Edelbrock, Rende, Plomin, & Thompson, 1995; Goodman &
Stevenson, 1989a, 1989b; Judy et al., 1997; Sherman, Iacono, &
McGue, 1997; Silberg et al., 1996; Stevenson, 1992; Thapar,
Hervas, & McGuffin, 1995).
More important, twin studies have used mathematical modeling
techniques to test directly the hypothesis that the clinical diagnosis
of ADHD is the extreme of a quantitative trait. Gjone, Stevenson,
and Sundet (1996) applied a mathematical model to determine if
the heritability of attention problems increased with their severity.
If ADHD accounted for the heritability of the broader dimension
of attention problems, then heritability should increase with in-
creasing severity. However, Gjone et al. found that heritability did
not change with severity. They concluded that there was in the
population a continuously distributed dimension of genetic liabil-
ity to attention problems. A similar approach was applied by Levy
et al. (1997). Like Gjone et al., they concluded that, with regard to
the genetic components of its etiology, ADHD was best viewed as
the extreme of a behavior that varies genetically throughout the
entire population rather than as a categorical disorder.
Although available data support the idea that ADHD can be
viewed as the extreme expression of a trait that varies quantita-
tively in the population, clinicians need ADHD symptom thresh-
olds for clinical purposes as much as blood pressure thresholds are
needed to define hypertension. Our data cannot provide the opti-
mal symptom threshold for adult ADHD, but they do highlight the
need for future research to examine this issue in more detail.
Our results must be considered in the context of some method-
ologic limitations. We do not know to what degree our findings
will generalize to nonreferred ADHD children in the community,
and although raters were blind to the diagnosis of the probands
parents were not. Moreover, the retrospective assessments of
childhood-onset ADHD and the assessments of current ADHD
symptoms were made by the same interviewer. Thus, it is possible
that the interviewer's knowledge of the adult's childhood symp-
toms might have contaminated the interviewer's ratings of the
adult's current symptoms. This possibility cannot account for the
differences we observed between child and adult relatives, but it
might have led to an overestimate of current ADHD symptoms in
adults who reported childhood symptoms.
Another limitation of our work is that we did not collect parental
reports or school records to confirm our retrospective diagnoses of
ADHD. It is possible that troubled adults who have been influ-
enced by media reports of ADHD may recognize ADHD symp-
toms in themselves, and this might bias their recall of childhood
symptoms. One safeguard against such bias was our use of a
control group, because such biases should have equally affected
the adults from ADHD and control families. Nevertheless, future
studies of adult ADHD would further strengthen the knowledge
base about adult ADHD by collecting informant reports or school
records of childhood symptoms.
Despite these limitations, our two family studies of ADHD boys
and girls provide further support for the hypothesis that ADHD is
more familial in adult samples. This finding shores up the validity
of retrospective diagnoses of adult ADHD and suggests that,
compared with the childhood diagnosis, the adult diagnosis may be
more valid and thus more informative for studies of the disorder.
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Appendix
DSM-III-R ADHD
Inattentive symptoms
Shifts activities
Difficulty sustaining attention
Difficulty following instructions
Easily distracted
Loses things
Does not listen
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Symptom Clusters
Hyperactive/impulsive symptoms
Difficulty remaining seated
Is fidgety
Has difficulty playing quietly
Talks excessively
Interrupts
Blurts out
Difficulty waiting turn
Acts before thinking
Received May 24, 1999
Revision received January 24, 2000
Accepted January 31, 2000 •